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Coronavirus disease (COVID-19) has aggressively spread across the United States with numerous fatalities. Risk factors for mortality are poorly described. This was a multicentered cohort study identifying patient characteristics and diagnostic markers present on initial evaluation associated with mortality in hospitalized COVID-19 patients. Epidemiological, demographic, clinical, and laboratory characteristics of survivors and non-survivors were obtained from electronic medical records and a multivariable survival regression analysis was conducted to identify risk factors of in-hospital death. Of 1629 consecutive hospitalized adult patients with confirmed COVID-19 from March 1st thru March 31, 2020, 1461 patients were included in final analysis. 327 patients died during hospitalization and 1134 survived to discharge. Median age was 62 years (IQR 50.0, 74.0) with 56% of hospitalized patients under the age of 65. 47% were female and 63% identified as African American. Most patients (55%) had either no or one comorbidity. In multivariable analysis, older age, admission respiratory status including elevated respiratory rate and oxygen saturation ≤ 88%, and initial laboratory derangements of creatinine > 1.33 mg/dL, alanine aminotransferase > 40 U/L, procalcitonin > 0.5 ng/mL, and lactic acid ≥ 2 mmol/L increased risk of in-hospital death. This study is one of the largest analyses in an epicenter for the COVID-19 pandemic. Older age, low oxygen saturation and elevated respiratory rate on admission, and initial lab derangements including renal and hepatic dysfunction and elevated procalcitonin and lactic acid are risk factors for in-hospital death. These factors can help clinicians prognosticate and should be considered in management strategies.

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Acute lung injury (ALI) is a life-threatening clinical syndrome in critically ill patients. The identification of novel biological markers for the early diagnosis of ALI and the development of more effective treatments are topics of current research. High mobility group box-1 protein (HMGB1) is a late inflammatory mediator associated with sepsis, malignancy, and immune disease. Levels of HMGB1 may reflect the severity of inflammation and tissue damage, indicating a potential role for HMGB1 as a prognostic biomarker in ALI, and a potential target for blocking inflammatory pathways. Several studies have shown that HMGB1 regulates autophagy. Autophagy, or type II programmed cell death, is an essential biological process that maintains cellular homeostasis. Studies have shown that HMGB1 and autophagy are involved in the pathogenesis of many lung diseases including ALI but the specific mechanisms underlying this association remain to be determined. This review aims to provide an update on the current status of the role of HMBG1 and autophagy in ALI.

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